The Curcumin Analogue, EF-24, Triggers p38 MAPK-Mediated Apoptotic Cell Death via Inducing PP2A-Modulated ERK Deactivation in Human Acute Myeloid Leukemia Cells

Hsiao, Pei Ching; Chang, Jer‐Hwa; Lee, Wei Jiunn; Ku, Chia-Chi; Tsai, Meng Ying; Yang, Shun Fa; Chien, Ming Hsien

doi:10.3390/cancers12082163

Cited by 23 publications

(27 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cells were then stained for 15 min at RT in the dark. The ratio of oral cancer cell apoptosis was evaluated by using the FITC Annexin V Apoptosis Detection Kit (BD Biosciences, San Jose, CA, USA) as previously described [19].…”

Section: Annexin V-fitc Staining Assaymentioning

confidence: 99%

Magnolol Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells through JNK1/2 and p38 Pathways

Chen

Lin

et al. 2021

Biomedicines

Self Cite

View full text Add to dashboard Cite

Magnolol is a natural compound extracted from Chinese herbal medicine and can induce apoptosis in numerous types of cancer cells. However, the molecular mechanisms of magnolol in oral cancer are still unclear. In this study, we investigated the anti-cancer effects and underlying mechanisms of magnolol in human oral cancer cell lines. Our results exhibited that magnolol inhibited the cell proliferation via inducing the sub-G1 phase and cell apoptosis of HSC-3 and SCC-9 cells. The human apoptosis array and Western blot assay showed that magnolol increased the expression of cleaved caspase-3 proteins and heme oxygenase-1 (HO-1). Moreover, we proved that magnolol induces apoptosis in oral cancer cell lines via the c-Jun N-terminal kinase (JNK)1/2 and p38 pathways. Overall, the current study supports the role for magnolol as a therapeutic approach for oral cancer through JNK1/2- and p38-mediated caspase activation.

show abstract

Section: Annexin V-fitc Staining Assaymentioning

confidence: 99%

Magnolol Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells through JNK1/2 and p38 Pathways

Chen

Lin

et al. 2021

Biomedicines

Self Cite

View full text Add to dashboard Cite

show abstract

“…Curcumin is known to play a role in anti-proliferation via modulating the MAPK signaling (Binion et al., 2008 ; Yallapu et al., 2014 ; Hsiao et al., 2020 ). We have further investigated whether the encapsulated curcumin function for mediating the anti-proliferation was through down-regulating p-MEK1/2 and p-ERK1/2 ( Figure 5(c) ), and the corresponding quantification is shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Synergistic effect of the anti-PD-1 antibody with blood stable and reduction sensitive curcumin micelles on colon cancer

Gong

Jia

et al. 2021

Drug Delivery

View full text Add to dashboard Cite

Curcumin (1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) is a potent anticancer drug with versatile biological activities, while the clinical translation of curcumin is severely limited due to its hydrophobicity, rapid elimination, and metabolism in the blood circulation. Herein, we aim to unravel the potential of curcumin as a synergistic agent with immunotherapy in the treatment of cancers. In an effort to minimize premature release and improve the systemic bioavailability, a superior blood stable and reduction sensitive curcumin micellar formulation, of which the release can be triggered by cancer cells, is rationally designed. We have synthesized a telodendrimer (mPEG-PLA-(LA) 4 ) capable of forming reversible disulfide crosslinked micelles (DCMs). The curcumin loaded DCMs (Cur/DCMs) are spherical with a uniform size of 24.6 nm. The in vitro release profile demonstrates that curcumin releases significantly slower from DCMs than that from non-crosslinked micelles (NCMs), while the release can be accelerated with the increasing concentration of reducing agent glutathione (GSH). Intravenous administration of Cur/DCMs stably retains curcumin in the bloodstream and efficiently improves the systemic bioavailability. Furthermore, Cur/DCMs exhibit synergistic anticancer efficacy when combined with the anti-PD-1 antibody in an MC-38 colon cancer xenograft model. Our results potentiate the integration of blood stable curcumin nanoformulation and immunotherapy for cancer treatment.

show abstract

“…Moreover, DMC has better anti-inflammatory and anticancer activity compared to curcumin (21,22). DMC reduced the viable cell number of human leukemia cells (16). Recently, we found that DMC reduced tumor weight and volume of HeLa cell xenograft mice in vivo (15).…”

Section: Discussionmentioning

confidence: 98%

“…Cells were cultured in IMDM medium supplemented with 10% FBS, 2 mM L-glutamine, and antibiotics (100 units/ml penicillin and 100 μg/ml streptomycin) in 75-cm 2 flasks and placed at 37˚C in a 5% CO 2 humidified atmosphere. The cultured medium was changed every two days (16).…”

Section: Methodsmentioning

confidence: 99%

“…Recently, we found that DMC significantly reduced tumor weight and volume of HeLa cell-xenograft mice in vivo (15). Moreover, DMC has been shown to decrease the proportion of viable cells in human AML cell lines (HL-60, U937, and MV4-11) (16). However, there are no further reports regarding the effects of DMC on the immune response of leukemia animal models in vivo.…”

Section: (Nk) Cells Furthermore Dmc Decreased B and T Cell Proliferation At High Doses Conclusion: Dmc Elevated Macrophage Phagocytosis Imentioning

confidence: 99%

See 1 more Smart Citation

Demethoxycurcumin Promotes Macrophage Cell Population and Phagocytosis in WEHI-3 Cell-generated Leukemia BALB/c MiceIn Vivo

Lin

Chen

Hsueh

et al. 2021

In Vivo

View full text Add to dashboard Cite

Background/Aim: Demethoxycurcumin (DMC), one of the components of curcuminoids, has antitumor activities in many human cancer cells and is known to induce apoptosis in human leukemia cells. However, there are no reports showing the effects of DMC on the immune response in leukemia mice in vivo. Herein, we evaluated the impact of DMC on immune responses in WEHI-3-generated leukemia mice in vivo. Materials and Methods: Fifty male BALB/c mice were separated randomly into five groups. Group I is normal mice, and groups II-V mice of generated leukemia by WEHI-3 cells. Group II-V mice were intraperitoneally injected with dimethyl sulfoxide (DMSO, as the positive control), 15, 30, and 60 mg/kg of DMC, respectively, every two days for 14 days. The body weight, blood, peritoneal fluid, liver, and spleen were individually analyzed. Results: DMC did not significantly affect animal appearance and body weight. It decreased liver and spleen weight at a high dose. DMC did not affect the cluster of differentiation 3 (CD3) and CD19 cell populations but induced decrease of CD11b at 30 mg/kg treatment. However, DMC at low dose significantly increased the cluster of macrophage (Mac-3) cell populations, but at high dose it decreased them. DMC increased macrophage phagocytosis from peripheral blood mononuclear cells at 15 mg/kg treatment and peritoneal cavity at 15, 30 and 60 mg/kg of DMC treatments. DMC did not significantly affect the cytotoxic activity of natural killer 3253 This article is freely accessible online.

show abstract

The Curcumin Analogue, EF-24, Triggers p38 MAPK-Mediated Apoptotic Cell Death via Inducing PP2A-Modulated ERK Deactivation in Human Acute Myeloid Leukemia Cells

Cited by 23 publications

References 53 publications

Magnolol Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells through JNK1/2 and p38 Pathways

Magnolol Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells through JNK1/2 and p38 Pathways

Synergistic effect of the anti-PD-1 antibody with blood stable and reduction sensitive curcumin micelles on colon cancer

Demethoxycurcumin Promotes Macrophage Cell Population and Phagocytosis in WEHI-3 Cell-generated Leukemia BALB/c MiceIn Vivo

Contact Info

Product

Resources

About